Hypertension is an unequivocally important risk factor for cardiovascular morbidity and mortality, an association strengthened by the presence of left ventricular hypertrophy. Though not proven, therapy successful in regressing hypertrophy may concurrently reduce its associated excess risk. However, the relationship between blood pressure and left ventricular mass is poor and the ability of effective antihypertensive therapy to regress cardiac mass is variable and drug-specific, leaving the stimulus to hypertrophy uncertain. this dissociation between hemodynamics and left ventricular mass has prompted investigation of additional factors - the sympathetic nervous system or the renin-angiotensin system - that may modulate ventricular growth in hypertension or in response to antihypertensive therapy. However, conventional analyses may underestimate the hemodynamic contribution to the hypertrophic process. The total load imposed on the left ventricle includes both steady-flow and pulsatile components. The former represents the cost of delivering the required cardiac output to the tissues. The latter, a consequence of the intermittent nature of the left ventricle as a pump, represents energy needed to overcome the inertial, elastic and reflective characteristics of the arterial system and is generally ignored in classic steady-flow hemodynamic analyses. With aging and in hypertension, the elastic elements of the vasculature deteriorate in response to unremitting cyclical stresses resulting in stiffening of the compliance vessels which may thereby impose an undetected, increased pulsatile load on the left ventricle. Aortic input impedance provides a measure of the total load placed on the left ventricle by the vasculature. Recent advances in technology allow for reliable measurement of aortic input impedance in small animals. The current proposal will utilize measurement of aortic input impedance and pulse wave velocity in normotensive and spontaneously hypertensive rats in order to test the hypothesis that a time-dependent increase in the pulsatile component of left ventricular load is responsible for the "physiologic" ventricular hypertrophy of aging in the absence of hypertension and for the progressive hypertrophy seen in hypertension despite a constant level of blood pressure elevation. The hypothesis that the differential effect of various antihypertensive agents on regression of ventricular hypertrophy relates to a variable effect on the vasculature and thereby on pulsatile load will also be tested. The principal investigator is a clinically-trained cardiologist committed to a career in academic research with a primary focus on the interaction between ventricular mass, function and load in hypertension and following myocardial infraction. A graduate of the Brigham and Women's Hospital training programs in Internal Medicine and Cardiology, he is well aware of the individuals and facilities available to a developing researcher in the Harvard medical area and takes full advantage of this unique opportunity.